摘要
目的明确银丹心脑通对脑缺血再灌注时神经细胞凋亡的保护作用,探索其治疗缺血性脑卒中的分子作用机制。方法将40只SD雄性大鼠按随机数字表法分为假手术组、模型组、阳性对照组(尼莫地平组1、银丹心脑通组。尼莫地平组及银丹心脑通组预先连续灌胃给药7d,假手术组和模型组每日灌服相当量的蒸馏水,第8天制备大鼠大脑中动脉阻塞模型。脑缺血再灌注24h后应用TUNEL法检测各组大鼠海马CAl区凋亡阳性神经细胞数,应用免疫组化染色测定各组大鼠脑组织中天冬氨酸特异性半胱氨酸蛋白酶.3(Caspase-3)的表达。结果模型组大鼠均能见到较多的凋亡阳性细胞数及Caspase-3阳性细胞数.与假手术组比较差异有统计学意义俨〈0.05):与模型组比较.银丹心脑通组、尼莫地平组能明显减小凋亡阳性细胞数及Caspase-3阳性细胞数,差异有统计学意义(P〈0.05);银丹心脑通组与尼莫地平组在凋亡阳性神经细胞数及Caspase-3阳性细胞数上比较差异无统计学意义(P〉0.05)。结论银丹心脑通对脑缺血再灌注损伤有一定保护作用,能够减少脑缺血再灌注大鼠神经细胞的凋亡,其作用机制可能与减少脑组织中Caspase-3的表达有关。
Objective To investigate the protective effects of Yindan Xinnaotong (YDXNT) on neural cell apoptosis in the hippocampus CA1 regions of rats with cerebral ischemia reperfusion and discuss the molecule mechanism of YDXNT treatment in cerebral ischemia. Methods Forty male Sprague-Dawley rats were randomly divided into sham-operated group, model group, positive control group (nimodipine treatment group) and YDXNT treatment group. Pretreatment by continuous intragastric administration for 7 days were given to the rats in the nimodipine treatment group and YDXNT treatment group, while rats in the sham-operated group and model group daily were fed with isovolumic distilled water. Middle cerebral artery models were established by a modified Longa occlusion method in the eighth day. Positive cell population in the hippocampus CA1 region of rats with ischemia 2 h and reperfusion 24 h was marked by TUNEL, and the caspase-3 expression was measured by immunohistochemical method. Results As compared with that in the control group, the number of apoptosis and Caspase-3-positive cells was significantly increased (P〈0.05), decreased number of apoptosis and Caspase-3-positive cells in the YDXNT treatment group and nimodipine treatment group was noted as compared with that in the vihicle group (P〈0.05); however, no difference of them between the nimodipine treatment group and YDXNT treatment group was noted (P〉0.05). Conclusion YDXNT has some protective effect on rats with brain ischemia reperfusion injury, by reducing cellpopulation of apoptosis, whose effect may be related to the reduced expression of Caspase-3.
出处
《中华神经医学杂志》
CAS
CSCD
北大核心
2013年第6期588-591,共4页
Chinese Journal of Neuromedicine
基金
遵义市科技局社会发展攻关项目(遵市科合社字[2012]39号)